[http://2009.igem.org/Team:Stanford/ProjectPage The 2009 Stanford iGEM Team] project centered on probiotics and Inflammatory Bowel Disease (IBD). IBD, as explained, is caused by an imbalance of two types of T-cells, Treg cells that immunosuppres the Th17 cells that cause the inflammation seen in patients. They suggest that an novel theraputic mechanism can be achieved by ''in vivo'' regulation of these cells. Their approach focuses in constructing two different ''Escherichia coli'', ''E.coli'', strains, each that would contain a distinct input/output cassette , each that is referred as a device.

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[http://2009.igem.org/Team:Stanford/ProjectPage The 2009 Stanford iGEM Team] project centered on probiotics and Inflammatory Bowel Disease (IBD). IBD, as explained, is caused by an imbalance of two types of T-cells, Treg cells that immunosuppres the Th17 cells that cause the inflammation seen in patients. They suggest that an novel theraputic mechanism can be achieved by ''in vivo'' regulation of these cells. Their approach focuses in constructing two different ''Escherichia coli'', ''E.coli'', strains, each that would contain a distinct input/output cassette , each that is referred as a device. The first device would detect as input Nitric Oxide, a byproduct of inflammation and Th17 proliferation, produces retinoic acid, that blocks further CD4+ T-cells differentiation into Th17 cells. The second device detects 5-Methyl tryptophan as an input and produces Interleukin-6 to regulate Treg proliferation to regulate their immunosuppression response. Ideally depending on the balance between these two markers, they would be able to cause differ

== Probiotics and the Media links ==

== Probiotics and the Media links ==

Revision as of 00:42, 18 March 2013

Contents

Probiotics

A probiotic (from the Latin, pro-, "in favor, for" and the Greek , biōtikós, "pertaining to life")refers to live microorganism that provides a benefit to the host, either directly or indirectly, by via interactions with the hosts cells or the host's microbiota. Such microorganism will interact by producing bioactives, biological compounds and macromolecules, that will produce such benefit.Although the concept of a probiotic has evolved since the the last century and the the first years of the current century that it acquired the current definition and we can see the health benefits humans can gain from he understanding of such interactions. Some research currently ongoing include the Human Microbiome Project[], and the use on single organisms to prevent disease. For example, the use of fecal transplantation for antibiotic-associated diarrea[].

Probiotics: Why we care.

To understand the reason why we care about probiotics, at how we gained our current understanding of the microbiota and the relation that exists mainly by studying the gut microbiota.

=== Gut microbiome and its benefits ====

The gut flora can be seen as a collection of bacteria[] This currently has been expanded to include also archea, fungi, and viruses.

The gut microbiome is described as a complex system of microbe-microbe and host-microbe interactions that exist in stable populations.

The advent of antiomicrobials and antibiotics that cause dysbiosis [] and leads to observation of "bacterial barrier" that prevents other microorganisms to colonize the gut.

Use of Probiotics: Present and Future

Oversight of Probiotics

iGEM 2009: Stanford's Approach to Probiotics

The 2009 Stanford iGEM Team project centered on probiotics and Inflammatory Bowel Disease (IBD). IBD, as explained, is caused by an imbalance of two types of T-cells, Treg cells that immunosuppres the Th17 cells that cause the inflammation seen in patients. They suggest that an novel theraputic mechanism can be achieved by in vivo regulation of these cells. Their approach focuses in constructing two different Escherichia coli, E.coli, strains, each that would contain a distinct input/output cassette , each that is referred as a device. The first device would detect as input Nitric Oxide, a byproduct of inflammation and Th17 proliferation, produces retinoic acid, that blocks further CD4+ T-cells differentiation into Th17 cells. The second device detects 5-Methyl tryptophan as an input and produces Interleukin-6 to regulate Treg proliferation to regulate their immunosuppression response. Ideally depending on the balance between these two markers, they would be able to cause differ